Teratogenic effects of maternal biotin deficiency on mouse embryos examined at midgestation.
Pregnant mice were fed a basal diet that not only did not contain biotin, but also contained the spray-dried egg white including avidin that caused the biotin deficiency. The effects of maternal biotin deficiency on craniofacial and limb development in embryos were examined at two stages of midgestation. On day 12.6 of gestation, male and female embryos weighted less and digit development was retarded in the biotin-deficient group. On day 15.6 of gestation (dg), the embryos also weighted less and external malformations, such as micrognathia (94.8%), micromelia (41.4%), and exencephaly (11.4%), were observed. The inhibition of palatal and digit formation by biotin deficiency at midgestation is responsible for later formation of cleft palate and micromelia. On dg 12.6 the liver biotin level of biotin-deficient dams was reduced to 20% of control values. Interestingly, the biotin content of the whole embryonic body was about ninefold greater than liver biotin levels in their dams.
Watanabe
T
T
Department of Hygiene and Preventive Medicine, Yamagata University School of Medicine, Japan.
Endo
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A
D000818:Animals; D001710:Biotin / Q000172:deficiency*; D001848:Bone Diseases, Developmental / Q000209:etiology; D002972:Cleft Palate / Q000196:embryology; D005314:Embryonic and Fetal Development; D005260:Female; D051379:Mice; D008813:Mice, Inbred ICR; D011247:Pregnancy; D011248:Pregnancy Complications
D001710:Biotin